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H2S and Pain: A Novel Aspect for Processing of Somatic, Visceral and Neuropathic Pain Signals

  • Chapter
Chemistry, Biochemistry and Pharmacology of Hydrogen Sulfide

Part of the book series: Handbook of Experimental Pharmacology ((HEP,volume 230))

Abstract

Hydrogen sulfide (H2S) formed by multiple enzymes including cystathionine-γ-lyase (CSE) targets Cav3.2 T-type Ca2+ channels (T-channels) and transient receptor potential ankyrin-1 (TRPA1). Intraplantar and intracolonic administration of H2S donors promotes somatic and visceral pain, respectively, via activation of Cav3.2 and TRPA1 in rats and/or mice. Injection of H2S donors into the plantar tissues, pancreatic duct, colonic lumen, or bladder causes T-channel-dependent excitation of nociceptors, determined as phosphorylation of ERK or expression of Fos in the spinal dorsal horn. Electrophysiological studies demonstrate that exogenous and/or endogenous H2S facilitates membrane currents through T-channels in NG108-15 cells and isolated mouse dorsal root ganglion (DRG) neurons that abundantly express Cav3.2 and also in Cav3.2-transfected HEK293 cells. In mice with cerulein-induced pancreatitis and cyclophosphamide-induced cystitis, visceral pain and/or referred hyperalgesia are inhibited by CSE inhibitors and by pharmacological blockade or genetic silencing of Cav3.2, and CSE protein is upregulated in the pancreas and bladder. In rats with neuropathy induced by L5 spinal nerve cutting or by repeated administration of paclitaxel, an anticancer drug, the neuropathic hyperalgesia is reversed by inhibitors of CSE or T-channels and by silencing of Cav3.2. Upregulation of Cav3.2 protein in DRG is detectable in the former, but not in the latter, neuropathic pain models. Thus, H2S appears to function as a nociceptive messenger by facilitating functions of Cav3.2 and TRPA1, and the enhanced function of the CSE/H2S/Cav3.2 pathway is considered to be involved in the pancreatitis- and cystitis-related pain and in neuropathic pain.

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Authors and Affiliations

  1. Division of Pharmacology and Pathophysiology, Kinki University School of Pharmacy, Higashi-Osaka, 577-8502, Japan

    Yuka Terada & Atsufumi Kawabata

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  1. Yuka Terada
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  2. Atsufumi Kawabata
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Correspondence to Atsufumi Kawabata .

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  1. National University of Singapore, Singapore, Singapore

    Philip K. Moore

  2. ST. Luke's Campus, University of Exeter Medical School, Exeter, United Kingdom

    Matt Whiteman

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Terada, Y., Kawabata, A. (2015). H2S and Pain: A Novel Aspect for Processing of Somatic, Visceral and Neuropathic Pain Signals. In: Moore, P., Whiteman, M. (eds) Chemistry, Biochemistry and Pharmacology of Hydrogen Sulfide. Handbook of Experimental Pharmacology, vol 230. Springer, Cham. https://doi.org/10.1007/978-3-319-18144-8_11

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